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By M. Sahay

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Introduction It is widely accepted that manifestation of target organs damage in patients with metabolic syndrome (MS) often has simultaneous and rapid pattern. Non-alcoholic fatty liver disease (NAFLD) has been described as one of metabolic syndrome-induced target organ damage. NAFLD clinical manifestations vary from ultrasonographically detected liver steatosis to non-alcoholic steatohepatitis (NASH) (Sowers, 2008). Detailed analysis of NAFLD relationship with other organs impairment in MS patients is particularly important for diagnostic procedures adjustment and optimization of treatment.

Novel OCRL mutations in patients with Dent-2 disease. J Pediatr Genet, in press Dent’s Disease 27 Bökenkamp A, Böckenhauer D, Cheong HI, Hoppe B, Tasic V, Unwin R, Ludwig M. (2009). Dent-2 disease: A mild variant of Lowe Syndrome. J. Pediatr, 155, pp. 94-99, ISSN 0022-3476 Bothwell SP, Farber LW, Hoagland A, Nussbaum RL. (2010). Species-specific difference in expression and splice-site choice in Inpp5b, an inositol polyphosphate 5phosphatase paralogous to the enzyme deficient in Lowe syndrome. Mammal Genome, 21, pp.

Hence, some residual activity of these smaller products might contribute to the phenotypic differences observed. , 2011). g. in the promoter or an intron, thereby leading to a decrease in expression or a cryptic splice product). On the other hand, a defect in another gene phenocopying Dent’s disease might be responsible. Four candidate genes (CLCN4, CFL1, SLC9A6, TMEM27) have been investigated so far. Dent’s Disease 23 CLCN4, the gene encoding ClC-4 has been analyzed (Ludwig and Utsch, 2004; Hoopes et al.

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